Cardiovascular diseases (CVD) are the leading causes of mortality in all gender and racial/ethnic groups of the U.S. population. The level and profile of postprandial lipids are important determinants of CVD risk. The mechanisms controlling postprandial lipid concentrations are not fully characterized and new evidence indicates that orosensory stimulation with dietary fat leads to a higher peak and more prolonged elevation of triglycerides (TO) after a lipid meal than stimulation with a non-fat food or no oral stimulation. Consequently, orosensory stimulation by dietary fat may contribute to CVD risk. The proposed studies will A) determine features of the oral stimulus (e.g., sensory properties, macronutrient content) that activate processes leading to augmented TG concentrations, B) ascertain whether orosensory stimulation exerts a differential effect on lipids varying in degree of saturation, C) identify individual characteristics (e.g., basal TG concentration, physiological responsiveness to sensory stimulation, selected personality traits) that may account for individual variability in lipid profiles, D) document the effects of orosensory stimulation on levels of particles associated with CVD risk (e.g., very-low-density- (VLDL) and intermediate-density-lipoproteins (IDL)), and E) establish whether orosensory stimulation augments the TG concentration by increasing lipid absorption and secretiOn from the gastrointestinal track, stimulating TG synthesis and secretion from the liver and/or reducing TG clearance. Salient features of oral stimuli and lipid loads will be assessed by monitoring blood constituents following manipulations of certain attributes. Individual characteristics that may be associated with heightened TO responsiveness to orosensory stimulation will be identified by contrasting findings obtained with individuals varying on selected traits. An improved understanding of the health risks related to orosensory stimulation by dietary lipids will be obtained by measuring lipid fractions associated with CVD risk. The mechanism underlying an orosensory influence on TG concentration will be clarified through control of lipid loading (gastric versus intravenous) and measurement of specific apoproteins (apoB-48, apoB-100) and a marker, retinyl palmitate.